2011
Increased Tubular Proliferation as an Adaptive Response to Glomerular Albuminuria
Guo JK, Marlier A, Shi H, Shan A, Ardito TA, Du ZP, Kashgarian M, Krause DS, Biemesderfer D, Cantley LG. Increased Tubular Proliferation as an Adaptive Response to Glomerular Albuminuria. Journal Of The American Society Of Nephrology 2011, 23: 429-437. PMID: 22193389, PMCID: PMC3294312, DOI: 10.1681/asn.2011040396.Peer-Reviewed Original ResearchMeSH KeywordsAlbuminuriaAnimalsAxl Receptor Tyrosine KinaseCell ProliferationDisease Models, AnimalFemaleHeparin-binding EGF-like Growth FactorIntegrasesIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsKidney GlomerulusKidney Tubules, ProximalMaleMembrane ProteinsMiceMice, TransgenicPodocytesProteinuriaProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesConceptsGlomerular proteinuriaTubular injuryTubular proliferationStructural glomerular injuryProteinuric renal diseaseOnset of albuminuriaRenal tubular atrophyDiphtheria toxin receptorRenal tubular cellsProximal tubule cellsGlomerular albuminuriaRenal failureSystemic inflammationTubular damageProgressive glomerulosclerosisRenal diseaseTubular atrophyGlomerular injuryRenal responsePodocyte lossProliferative responseTubular cellsAnimal modelsProteinuriaReceptor Axl
2007
The commonly used β-actin-GFP transgenic mouse strain develops a distinct type of glomerulosclerosis
Guo JK, Cheng EC, Wang L, Swenson ES, Ardito TA, Kashgarian M, Cantley LG, Krause DS. The commonly used β-actin-GFP transgenic mouse strain develops a distinct type of glomerulosclerosis. Transgenic Research 2007, 16: 829-834. PMID: 17594530, DOI: 10.1007/s11248-007-9107-x.Peer-Reviewed Original Research